Kyushu University Academic Staff Educational and Research Activities Database
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Horisawa Kenichi Last modified date:2019.07.01





Academic Degree
Ph.D
Field of Specialization
Molecular Biology
Research
Research Interests
  • Analysis of the relationship between liver regeneration and metabolism
    keyword : Liver, Regeneration, Metabolism
    2018.08~2020.07.
  • Crosstalk between lipid metabolism and transcription
    keyword : lipid metabolism, transcription
    2016.04~2019.03.
  • Molecular elucidation of liver development and direct reprogramming of somatic cells to hepatocyte
    keyword : liver,organogenesis, direct reprogramming, epigenetics, proteomics
    2013.12~2018.11.
Academic Activities
Books
1. Horisawa Kenichi, Hiroshi Yanagawa, “Chapter 10: Musashi Proteins in Neural Stem/Progenitor Cells” Neural Stem Cells and Therapy, InTech, pp.205-222, 2012.02.
Reports
1. Horisawa Kenichi, Atsushi SUZUKI, Cell-Based Regenerative Therapy for Liver Disease, Innovative Medicine Basic Research and Development, Springer, 2015.10.
2. 堀澤 健一, Specific and quantitative labeling of biomolecules using click chemistry., Front Physiol., 2014.11.
3. Horisawa Kenichi, Takao Imai, Hideyuki Okano, Hiroshi Yanagawa, The Musashi family RNA-binding proteins in stem cells, Biomolecular Concepts, 2010.03.
Papers
1. Takashima Y, Horisawa K, Udono M, Ohkawa Y, Suzuki A., Prolonged inhibition of hepatocellular carcinoma cell proliferation by combinatorial expression of defined transcription factors., Cancer Sci. , 10.1111/cas.13798., 109, 11, 3543-3553, 2018.11.
2. Maiko Terada, Horisawa K, Shizuka Miura, 高島 康郎, Ohkawa, Y, Sayaka Sekiya, 松田 花菜江, Atsushi Suzuki, Kupffer cells induce Notch-mediated hepatocyte conversion in a common mouse model of intrahepatic cholangiocarcinoma., Sci Rep., doi: 10.1038/srep34691., 6, 34691-34691, 2016.10, Intrahepatic cholangiocarcinoma (ICC) is a malignant epithelial neoplasm composed of cells resembling cholangiocytes that line the intrahepatic bile ducts in portal areas of the hepatic lobule. Although ICC has been defined as a tumor arising from cholangiocyte transformation, recent evidence from genetic lineage-tracing experiments has indicated that hepatocytes can be a cellular origin of ICC by directly changing their fate to that of biliary lineage cells. Notch signaling has been identified as an essential factor for hepatocyte conversion into biliary lineage cells at the onset of ICC. However, the mechanisms underlying Notch signal activation in hepatocytes remain unclear. Here, using a mouse model of ICC, we found that hepatic macrophages called Kupffer cells transiently congregate around the central veins in the liver and express the Notch ligand Jagged-1 coincident with Notch activation in pericentral hepatocytes. Depletion of Kupffer cells prevents the Notch-mediated cell-fate conversion of hepatocytes to biliary lineage cells, inducing hepatocyte apoptosis and increasing mortality in mice. These findings will be useful for uncovering the pathogenic mechanism of ICC and developing prevenient and therapeutic strategies for this refractory disease..
Membership in Academic Society
  • Japanese proteomics society
  • The RNA society of Japan
  • The molecular Biology society of Japan
Educational
Educational Activities
Research advising for students
Other Educational Activities
  • 2014.06, Research advising for 3rd grade students in medical school.
  • 2015.06, Research advising for 3rd grade students in medical school.
  • 2017.06, Research advising for 3rd grade students in medical school.